Contribution of villous atrophy to reduced intestinal maltase in infants with malnutrition

J Pediatr Gastroenterol Nutr. 2000 May;30(5):494-502. doi: 10.1097/00005176-200005000-00007.


Background: It has been known for many years that small intestinal maltase activities are reduced in malnourished infants and in other patients with villous atrophy. The recent availability of human maltase-glucoamylase cDNA provides the opportunity to test the hypothesis that villous atrophy accounts for the reduced maltase enzyme activity in malnourished infants.

Methods: Mucosal biopsy specimens obtained for clinical evaluation of malnourished infants with poor responses to refeeding were examined by quantitative methods for enzyme activity and mRNA levels.

Results: Maltase activity and maltase-glucoamylase mRNA were reduced (approximately 45% of normal). When maltase-glucoamylase message was normalized to villin message, a structural protein expressed only in enterocytes, a preservation of maltase messages in surviving enterocytes was documented. The luminal glucose transporter-villin message was also preserved.

Conclusions: The loss of maltase-glucoamylase message paralleled the reduction in villin message and degree of villous atrophy. The reduced maltase-glucoamylase message also paralleled sucrase-isomaltase message, previously found to be decreased in proportion to villous atrophy of malnourished infants. The data directly demonstrate, for the first time, that the terminal steps of starch 1-4 starch digestion and sucrase-isomaltase 1-6 starch digestion are decreased in malnourished infants, secondary to villous atrophy. These data in prior and present reports suggest that mechanisms underlying the chronic villous atrophy of malnutrition should be a priority for investigations in malnourished infants with slower than expected weight gain during refeeding.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Actins / genetics
  • Atrophy
  • Biopsy
  • Carrier Proteins / genetics
  • Child, Preschool
  • Female
  • Humans
  • Infant
  • Intestinal Mucosa / enzymology
  • Intestinal Mucosa / pathology
  • Intestines / enzymology*
  • Intestines / pathology*
  • Male
  • Membrane Glycoproteins / genetics
  • Microfilament Proteins / genetics
  • Monosaccharide Transport Proteins / genetics
  • Nutrition Disorders / enzymology*
  • Nutrition Disorders / pathology*
  • Nutritional Status
  • RNA, Messenger / metabolism
  • Sodium-Glucose Transporter 1
  • alpha-Glucosidases / genetics
  • alpha-Glucosidases / metabolism*


  • Actins
  • Carrier Proteins
  • Membrane Glycoproteins
  • Microfilament Proteins
  • Monosaccharide Transport Proteins
  • RNA, Messenger
  • Sodium-Glucose Transporter 1
  • villin
  • alpha-Glucosidases